Volume 12, Number 2

Stasis Considered

Michael Thomas

Continuity and Discontinuity

The debate between evolutionists and creationists takes many
forms. Unfortunately, it usually centers around issues which are
peripheral to the main point of contention, namely, the existence
of two opposing perceptions of nature. For the evolutionist, the
living world is continuous and the lineages of all existing species
can be traced back ultimately to a single common ancestor. Inherent
in this theory of continuity is the claim that transformations
from one type to another are possible. Organisms must therefore
possess a sufficient amount of plasticity, which, over time, will
make it possible for them to realize such changes.

The creationist perceives the living world from an opposing
perspective. Instead of a continuous biological tree linking all
creatures, the creationist perceives a series of discrete groups
or types. Each type supposedly had an independent origin, and
the biochemical, morphological, and behavioral gaps which exist
between these types cannot be bridged by the processes proposed
by evolutionists. Creationists do not deny change; time, chance,
and natural forces are thought to be involved in the fluctuating
characteristics of organisms. These factors, however, are insufficient
to transform one type into another. Although the exact borders
which separate the types of organisms may at times be unclear,
sufficient evidence exists to support the idea of discontinuity
between types (Denton, 1985).

Inherent in the theory of discontinuity is the notion of stasis.
Put simply, stasis implies that certain mechanisms exist which
prevent an organism of a particular type from transforming to
the extent that it no longer belongs to its original type.

Preconceptions in Biology

Evolutionists have proposed a myriad of possible mechanisms
thought to generate the variation necessary for transformation
(Endler and McLellan, 1988). Such mechanisms include mutation,
random genetic drift, gene duplication, exon shuffling, and transposable
elements. Creationists, on the other hand, have offered few possible
mechanisms for stasis. Until such mechanisms are proposed, experimental
research guided by theories of discontinuity will suffer greatly.

The general absence of theoretical analyses or experimental
data supporting mechanisms of stasis does not, however, mean that
such mechanisms do not exist. Rather, for a long time the majority
of the biological community has worked under the preconception
of continuity: most biologists have been looking for, and attempting
to demonstrate, change in species. Writing about bacterial evolution
about ten years ago, Bennett and Richmond (1978: 54) candidly
admitted their preconceptions:

Of course, our outlook is biased since we are interested,
in general, in our ability to produce change; intuitively we
are less excited by mechanisms of maintaining the status quo.

Such preconceptions are best explained in Kuhnian terms (Kuhn,
1970). According to the historian of science Thomas Kuhn, science
does not proceed as an objective progression toward the truth.
Instead, it proceeds as a discontinuous series of unrelated paradigms.
Paradigms work to determine what facts are important, how the
facts should relate to theory, and aid in the articulation of
a theory (Kuhn, 1970: 34).

Put simply, paradigms define what is important in a science
at any time. And without a doubt, for over a century the principle
of continuity has served as the dominant paradigm in the biological
sciences. Thus, we see the preoccupation with demonstrating change
and integrating it into theories spawned by the paradigm of continuity.

The preconception of continuity goes a long way toward explaining
our general ignorance about mechanisms of stasis. At present the
proponents of discontinuity may have difficulty outlining mechanisms
of stasis, but this should not be surprising: no one has been
looking for such mechanisms!

In fact, the common preconception of continuity ought to spur
creationists on. For in spite of many decades of intensive world-wide
research into the mechanisms of transformation, it is apparent
that the payoff has been meager, especially when the origin of
higher taxa--i.e., macroevolution--is considered. Macroevolution
has never been experimentally demonstrated, nor has a satisfactory
mechanism for such transformations been established. Indeed, evolutionist
C.R. Woese (1987: 177) recently admitted:

[T]he term `macroevolution' serves more to hide our ignorance
than symbolize our understanding.

If macroevolution (which is predicted by continuity, but denied
by discontinuity) cannot be empirically demonstrated--in spite
of the fact that for decades the biological community has sought
just such a demonstration--perhaps it is time to consider discontinuity
and stasis as viable alternatives.

Evidence of Stasis

It is not merely the lack of evidence for macroevolutionary
transformations which suggests stasis; very good paleontological
and molecular data demonstrate the phenomenon. The fossil record
provides many examples. It is now recognized that once a species
appears in the fossil record, it remains for a long time relatively
unchanged. Stanley (1981: xv) writes:

The record now reveals that species typically survive for
a hundred thousand generations, or even a million or more, without
evolving very much.

A million generations and no change--this is an observable
fact, not an interpretation depending on a particular world view.
This stasis becomes even more apparent if living species are compared
to their fossil counterparts. Pierre Grasse (1977: 76-79) offers
a small sample from a rather large list of such species. One example
is the opposum (Didelphis). A comparison of living opposums
with their fossilized counterparts of 70 million years ago demonstrates
little change. Grasse (1977: 78) comments:

Yet the opposums, which live in such widely different environments
as damp forests, savannas, subdesert areas, and the edges of
town, are subjected to conditions theoretically favorable to
evolution. Some of their species...are widely distributed and
mutate extensively. They are quite healthy relics, but they refuse
to evolve.

When one realizes that the opposum is not a specialized animal,
it is surprising from the perspective of continuity that no significant
change has occurred in 70 million years.

Another example is the cockroach. When living cockroaches are
compared to fossilized cockroaches approximately 280 million years
old, little change is observed (Grasse, 1977: 87). In spite of
280 million years of mutations and changing environments, the
body plan of the cockroach has not changed. Furthermore, the phenomenal
reproductive rate of these organisms translates into a very large
gene pool. Surely many advantageous mutations should have been
selected for--yet the body plan has remained static.

Examples like these (see Eldredge and Stanley, 1984, for extensive
documentation) could be multiplied many times over and the theme
would remain the same. Species that have undergone millions of
years of mutations, situated in varying environments which ought
to be favorable to evolution, exhibit little or no change. Taken
at face value, the fossil record clearly demonstrates stasis:
we do not have to speculate about the reality of the phenomenon.

Molecular Data

The molecular evidence in support of stasis is equally convincing.
In 1983, Martin Kreitman looked at eleven copies of the gene for
alcohol dehydrogenase in Drosophila melanogaster (Kreitman,
1983). He found that 1.617% of the 2,659 nucleotides whichmake
up the gene are polymorphic. Of these polymorphic sites, only
14 were in coding regions (the remainder were in introns and flanking
regions), and of those 14, only one resulted in an amino
acid substitution. Using mathematical models, Kreitman determined
that an immense bias exists towards silent substitutions (i.e.,
nucleotide changes which do not effect the amino acid specified).

Why is it that most of the differences in nucleotide sequence
are found in noncoding regions of the gene? And for those differences
within coding regions, why are the majority of substitutions silent?
This bias is best explained by selection. Most mutations that
occur in coding regions will alter the amino acid specified, disrupting
proper function; hence, these mutations will be removed by selection.
The reason we do not see more variation in the coding regions
of genes is that the organisms carrying such mutations die (or
have greatly reduced fitness). It appears that the major role
of selection at the molecular level is that of a conserving, not
transforming, force.

This conclusion is supported by a wealth of other molecular
data. Clarke (1970) observed that for a particular protein, substitutions
(in a variety of species) which were accompanied by small chemical
changes were much more common that those associated with large
chemical changes. Bogardt et al. (1980) looked at mammalian
myoglobins; by making a residue-by-residue comparison and considering
various physico-chemical properties of amino acids, they found
that differences which are compatible with the retention of the
original conformation of the protein appear to be favored. Kimura
(1983) looked at the relationship between physico-chemical differences
and the relative frequency of amino acid differences among various
`homologous' proteins. He found a convincing negative correlation
between the two: the greater the physico-chemical difference associated
with a particular amino acid substitution, the smaller the rate
of occurrence of such events.

This theme is repeated from other perspectives. Molecules which
are functionally important show less dissimilarity between types
of organisms when compared to functionally less important molecules.
Extreme examples might include the fibrinopeptides and histones.
Fibrinopeptides, which have little known function after they become
separated from fibrinogen in the blood clot, demonstrate significant
differences between types. In contrast, histone proteins--which
play an essential role in DNA packaging--demonstrate little variability
between types. In fact, when the histone H 4 (approximately 100
amino acids) of pea plant and calf thymus are compared, only two
amino acid differences are seen (Isenburg, 1979). This is in spite
of the fact that plants and animals supposedly diverged 1.2 billion
years ago.

Different parts of the same molecule also demonstrate this
same theme. Amino acid sequences which play a crucial role in
the function of a particular protein demonstrate a rather stringent
conservation when compared to amino acid sequences which do not.

For example, Jukes (1971) looked at the amino acid sequences
of vertebrate hemoglobins spanning a supposed evolutionary history
of 500 million years. When he surveyed the position of the two
histidines which bind to the heme molecule (and thus function
importantly in the molecule), he found an almost complete invariance.

Among different types of organisms, functionally important
molecules and functionally important parts of molecules demonstrate
remarkable homogeneity: these molecules cannot tolerate significant
change. If such change occurs, selection will work to prevent
it from being propagated. As Fristrom and Clegg (1988: 689) explain:

[T]he great majority of mutations in genes whose products
play a central role in metabolism may disrupt function and lead
to deleterious conditions. Such mutations are rapidly eliminated
by selection and do not become part of the evolutionary record
of nucleotide substitutions.

In other words, the indirect effects of selection seem to indicate
that it works at the molecular level not as a force of major transformation,
but as a force of stasis. Obviously, the selection pressure remained
rather constant over time for all these important proteins.

One might argue that if selection pressures had changed, it
is possible that these proteins could have evolved away from their
basic types. To argue along these lines, however, is to place
the cart before the horse--for the data indicate that selection
pressures have not changed throughout nature and over hundreds
of millions of years.

Yet if numerous macroevolutionary events are behind the diversity
of the living world, surely many important molecules must have
changed radically. This seems unlikely, for randomly changing
the very things which are most resistant to change does not translate
into a very successful formula. At least that is what the molecular
data are telling us.

Gene Duplication

How can an important molecule or structure change when the
molecular data indicate that such transformations are doomed to
failure? How is one gene transformed into another gene, if such
changes will most often result in the loss of that gene, and thus
the reduced viability or death of the organism "experimenting"
with such changes? The most common explanation is the hypothesis
of gene duplication (Markert et al., 1975). Suppose that
a particular gene which encodes for protein A is duplicated. If
a functioning protein A is essential for the life of an organism,
random changes in the gene for that protein will be lethal. But
if there are now two copies of the gene, the situation is different.
The ancestral gene can continue coding for protein A and thus
important processes are maintained. The duplicate gene, howver,
is free to accumulate mutations which might ultimately transform
it into a different, functioning protein.

Such a hypothesis seems plausible. Three lines of reasoning,
however, suggest that this mechanism is probably insufficient
to generate enough new genetic material to account for all the
transformations which must have occurred.

First, consider the larger perspective. A common example of
putative gene duplication concerns the oxygen transport molecules
myoglobin and hemoglobin . Myoglobin is assumed to be the ancestral
molecule (where did it come from?). About 650 million years ago,
the myoglobin gene was supposedly duplicated, and the newgene
for [alpha] hemoglobin was formed. Subsequent duplications and
divergences led to the addition, in this gene `family,' of [beta]-hemoglobin,
[gamma]-hemoglobin, and [delta]-hemoglobin.

Yet even if this hypothesis is correct, not much change has
really occurred. Lester and Bohlin (1984: 91) comment:

After 650 million years of duplication and subsequent mutation,
the various genes have not escaped their basic function of oxygen
transport .Once an oxygen transporting gene, always an oxygen
transporting gene.

If such a transformation did occur, it was still constrained
by some form of stasis. What mechanisms of stasis might exist
to constrain these types of molecules from transforming into something
really different? I would now like to suggest two possible mechanisms
which cast doubt on the efficacy of gene duplication.

Protein Degradation

One mechanism which may counteract gene duplication is protein
degradation. Inside a cell, proteins do not exist in static pools.
Instead, they are in a dynamic state of constant turnover. New
proteins are made to replace old proteins (which are broken down).
Hershko and Ciechanover (1982) define several classes of cellular
proteins in terms of their degradative properties. Long-lived
proteins, which constitute the majority of cellular proteins,
have a slow turnover rate. Short-lived proteins have an exceptionally
high turnover rate. Abnormal proteins, which may arise from mutations
or errors in RNA/protein synthesis, are broken down more rapidly
than short-lived proteins.

The rate of degradation of abnormal proteins is impressive.
In E. coli, normal [beta]-galactosidase is completely stable,
but if incomplete chains are synthesized, they are broken down
in a few minutes (Zubay, 1988). Hemoglobin is a remarkably stable
molecule which lasts the life span of the red blood cell. However,
if a synthetic analog for the amino acid valine is incorporated
into the newly forming hemoglobin, the resulting polypeptide is
broken down with a half-life of about ten minutes. According to
Zubay (1988: 968), cells have "very efficient mechanisms
to recognize and quickly degrade the damaged proteins."

One polypeptide thought to play an important role in eukaryotic
protein degradation is ubiquiton (Zubay, 1988: 968). Ubiquiton
has been detected in all eukaryotes examined and its amino acid
sequence is remarkably conserved (Hershko and Ciechanover, 1982).
It works by covalently linking, in an ATP-dependent series of
reactions, to the lysine residues of abnormal proteins. This linking
marks the protein for rapid degradation by other cellular proteases.

Although such processes are just beginning to be elucidated,
it is quite apparent that they play a crucial and finely controlled
role in the life of the cell. Their significance is obvious: by
preserving the status quo, these processes seriously challenge
notions of transformation at the molecular level.

If gene duplication is to have any relevance, novel proteins
ultimately had to be formed. For example, the duplicated gene
may be copied in such a way that it is no longer expressed. At
this point, it would accumulate mutations at the rate of a pseudogene.
Some time later, the gene may then be `reactivated,' resulting
ultimately in the production of a novel protein. Although the
protein degradation processes would be irrelevant while the gene
is actually mutating, once the product is finally expressed their
role becomes evident. Since the duplicated gene mutated without
being expressed, selection could not edit this process. It is
highly likely that the gene product would be chaotic in structure
and thus be recognized by the protein degradation processes. And
even if the new protein were to escape those processes, it is
unlikely to be functional simply because it was "redesigned"
randomly.

I should also mention that there are difficult problems associated
with reactivating a silent gene. Li (1983: 29) argues:

[T]he probability of reactivation would still be very small...because
a pseudogene often contains multiple major defects such as frameshifts,
which cannot be easily corrected.

These problems seem to negate the effectiveness of this method
of gene duplication.

Another route is to allow the duplicated gene to continue expressing
its product constitutively as it undergoes mutation. Although
this route would bypass the problems associated with random changes
and reactivation, the gene product would be opposed constantly
by protein degradation processes. Most proteins exist in a three-dimensional,
globular state. But to change one form of protein into another
form would include a significant amount of gradual unfolding and
refolding. This process of unfolding and refolding is likely to
cue the degradative processes.

The protein degradation processes constitute a selective force
to constrain molecular structure and therefore function. Selection
would work to maximize the resistance to these proteases. And
how is this accomplished? Simply by minimizing the change in protein
structure. The less a protein changes, the lower the likelihood
that that protein will encounter degradation processes.

One should also note that these processes of protein degradation
use energy (Ciechanover et al., 1984). Any organism "experimenting"
with the production of abnormal proteins as a result of gene duplication
and mutation would be investing huge amounts of energy, just to
degrade these proteins during the long intervening period between
functional states. Any organism experimenting with protein modification
is likely to be at an energetic disadvantage compared to organisms
which minimized such "experiments."

It seems implausible that a new functional protein could form
randomly over thousands of years, when abnormal proteins are degraded
in minutes. Do abnormal proteins--usually degraded rapidly--really
constitute the raw materials of gradual evolution?

Gene Conversion

If gene duplication is to be a source of new functional proteins,
it must also overcome the DNA repair processes expressed in gene
conversion. To better understand the significance of gene conversion,
one should consider an interesting property of multigene families.

Many essential intracellular molecules are encoded for by multiple
copies of a gene. One example concerns the rRNA genes (Fristrom
and Clegg, 1988: 677). Approximately 600 copies of the rRNA genes
are found in the frog Xenopus, arranged on the chromosome
as tandem repeats. When the genes were mapped and seqeunced, a
striking discovery was made: the multiple copies within the
species were nearly identical.

How could this be? Surely mutations should have accumulated
in these multiple copies, creating significant differences among
them. What forces are at work to maintain the homogeneity of 600
copies of a particular gene?

Since rRNA genes are essential to the life of the organism,
changes are likely to be detrimental; selection, then, might appear
to be an obvious candidate. Given the great multiplicity of these
genes, however, it is hard to see how selection could work to
eliminate new mutations. For example, a mutation in one gene is
unlikely to have a perceptible effect because the non-functional
gene product is greatly outnumbered by the hundreds or thousands
of wild type, functional gene products.

The most widely accepted mechanism for maintaining this homogeneity
of multiple gene copies is gene conversion (Li et al.,
1985). Gene conversion is the consequence of heteroduplex formation
and DNA repair (see Figure 1). In essence, two sequences from
two different strands of DNA interact in such a way that one is
converted by the other. Where once there was diversity, there
is now homogeneity. Gene conversion works to maintain the homogeneity
of repeated sequences (see Figure 2, which illustrates only one
round of gene conversion). It should be obvious that this process
would continue until the mutation either spreads or is lost.

Now consider the process of gene duplication. Two identical
copies of a gene are made. This means that a multigene family
is being created! The door is now open for gene conversion to
work, in opposition to the functional divergence which the theory
of gene duplication assumes will follow. In other words, if one
copy of the duplicated gene undergoes mutation, gene conversion
will work to eliminate the resulting diversity. As Li et al.
(1985: 72) write:

[I]f there are only two repeats on a chromosome, a single
intrachromosomal gene conversion will lead to homogeneity of
the repeats on the chromosome.

Quantitative data exist to support this hypothesis. When the
mutation rate--which generates diversity--is compared to the rate
of gene conversion--which generates homogeneity--one finds that
the frequency of gene conversion is "clearly much higher
than the frequency of mutation" (Klein and Petes, 1981).
Douglas Futuyma (1983: 141) notes that an average gene mutates
at a rate of 10 -5 per generation. On the other hand, experimental
evidence demonstrates that the frequency of gene conversion is
approximately 10 -2 per generation (Klein and Petes, 1981; Klein,
1984). It is important to emphasize that such frequencies were
obtained by studying the interactions of only two copies of a
particular gene. This makes it possible to validly extrapolate
such frequencies to the post-gene duplication state (where two
copies of a particular gene exist). The evidence indicates that
gene conversion occurs one thousand times more often than the
mutation rate. Thus, it is highly improbable that on its way to
a novel function, a duplicated gene could continually escape gene
conversion processes.

It seems clear that gene conversion will maintain the original
allele. If gene conversion worked to spread the mutation to both
alleles instead of eliminating it, selection would likely eliminate
such changes. Remember the attractive feature of gene duplication
is that one gene can continue to produce its essential gene product
while the other is free to accumulate changes. But if gene conversion
spreads the mutations, this feature is lost. We are back to suggesting
that essential molecules can tolerate random changes .

Given the homogeneity of multigene families in spite of mutations,
gene conversion seems to be at work. And not only would it work
to maintain this homogeneity, it would oppose the divergences
which supposedly follow gene duplication, and thus would constitute
a mechanism of stasis.

Other Possible Mechanisms of Stasis

We have seen that stasis is evident in the fossil record and
in the molecular data. We have also seen that the popular notion
of gene duplication inadequately explains significant molecular
transformations. When all this is added to the absence of a working
mechanism for macroevolution, the case for continuity seems weak.
Perhaps it is time to consider seriously possible mechanisms of
stasis.

I propose that mutational changes must travel through several
levels of stasis before becoming fixed in a population. When these
mechanisms are considered in toto, it is unlikely that theories
of continuity can account for the diversity of body plans and
molecules we observe.

A battery of DNA repair enzymes and pathways make up the first
level of post-replicational stasis. Through a variety of mechanisms,
mutations are recognized and corrected to restore the original
nucleotide sequence (Kornberg, 1980: 607-624). Although these
mechanisms cannot drive the mutation rate to zero, they are finely
tuned to minimize it (Haynes, 1988: 577-584). The processes involved
in gene conversion are part of this level of stasis.

The second level of stasis is post-translational. As we have
already seen, a variety of protein degradation systems recognize
and eliminate abnormal proteins. For one type of organism to transform
into another type, some new proteins would have to be formed through
gradual mutation. Yet these biochemical reactions would serve
as a powerful force oppposing novel change.

The third level of stasis is nuclear-cytoplasmic. Regulatory
molecules which interact with the DNA may serve as a process which
prevents radical change and further retards the extremely slow
process of neo-Darwinian transformation. Experimental research
with nuclear transplants (which remove the nucleus from one cell,
and replace it with the nucleus from another cell) suggest this.

One illuminating experiment involved the removal of the nucleus
from the egg of the frog Xenopus laevis laevis (Gurdon,
1962). This enucleated egg then received the nucleus from the
embryo of Xenopus tropicalis. The resulting egg never developed
beyond the late neurula stage. If it received the nucleus from
an embryo of Xenopus laevis laevis, however, it developed
into an adult frog.

Other researchers conducted similar experiments with two protozoans,
Amoeba proteus and Amoeba discoides (Yudin, 1979).
When the nucleus from A. proteus was transplanted into an enucleated
cell of the same species, 90% of the cells survived. However,
if the nucleus from A. discoides was transplanted into
the enucleated cell of A. proteus, only 1% of the cells
survive. This phenomenon is known as transplantation incompatibility
(Yudin, 1979: 66).

Experiments like these clearly suggest that DNA alone is insufficient
to guide the development of an animal, or insure the survival
of protozoans. Cytoplasmic regulatory molecules probably exist
to decode the DNA. It is possible that there must be a correct
distribution of such molecules and/or the correct affinity for
the DNA if proper gene expression is to occur. What might be happening
is this: when the nucleus from species A is placed in the enucleated
cell of species B, the regulatory molecules in the cytoplasm of
B cannot properly decode the DNA of A. From such results, J.M.
Barry (1986) concludes:

The possibility is often overlooked that each generation of
organisms must inherit not only DNA from the previous generation
but also other cell components peculiar to that species.

This phenomenon would seem to preclude macromutations. For
example, if the DNA of an egg undergoes a major mutational reconstruction
which might now encode for a novel protein and/or pathway, it
is highly improbable that simultaneous mutations would produce
the necessary regulatory molecules to express these new features
properly. Yet if these unlikely mutations are not simultaneous,
the embryo will not develop successfully.

Barry (1986) argues, however, that this phenomenon does not
preclude neo-Darwinian evolution. He writes:

In the development of new species, mutations in DNA produce
changes in the structure of other cell components which in turn
allow the survival of further mutations in DNA.

Although this may look plausible in principle, when one considers
the extreme rarity of advantageous mutations in general, it certainly
appears that such a mechanism will be unable to generate the great
diversity of form and function found in nature. After all, you
can slow down a gradual process only so much before it becomes
undetectable.

The fourth level of stasis is populational. Assume that a mutation
occurs, somehow bypasses the DNA repair mechanisms and protein
degradation processes, and does not interfere with the cytoplasmic
regulatory mechanisms. Unless this mutation is advantageous, and
has a very high selective coefficient (rare events in themselves),
its frequency in a population will remain very low. Thus, these
alleles are likely to be lost by random drift (where the probability
of being lost is 1-1/2N, where 2N = the number of genes in a diploid
population).

Even if the mutation bypasses the cellular mechanisms of stasis,
spreads to a significant percentage of the population, and is
advantageous, major transformations still appear improbable. This
is because microevolutionary changes may be yet another
process that maintains stasis.

This may seem paradoxical. But a commonly cited example of
microevolution-- industrial melanism--will illustrate the point.
As a result of strong selective forces, the melanic forms of the
moth Biston betularia almost completely replaced the non-melanic
forms. Had Biston betularia lacked the requisite genetic
variability for color, the species may have become extinct. Too
much stasis is deleterious to a species. Limited variability,
on the other hand, works to allow the species to continue to exist
as that species under adverse conditions. After all, Biston
betularia responded to environmental challenges, and changed,
as Biston betularia. Microevolution works as a force of
stasis by allowing a species or type to continue to exist as
that species or type under modified environmental conditions.

Another example may be helpful. Bacteria exhibit remarkable
homogeneity in both morphology and biochemistry. Yet, on a lower
level, one may observe a striking amount of plasticity. Consider
antibiotic resistance: a bacterial colony normally sensitive to
an antibiotic may become resistant to that antibiotic. The antibiotic
streptomycin, for instance, interacts with bacterial ribosomes,
disrupting normal protein synthesis. Ordinarily, this disruption
will kill the affected bacteria. Yet some bacteria have mutations
in the genes for their ribosomal proteins, which allow their ribosomes
to function, unhindered by streptomycin (Zubay, 1988: 957).

Yet note that the mutated ribosome is still typically bacterial.
If the bacterial ribosome had become eukaryotic-like, streptomycin
resistance would also be observed--but bacteria change as bacteria,
not by transforming into another type. The minor biochemical changes
associated with such bacterial 'evolution' work to preserve the
bacteria type. Transformations to non-bacterial characteristics
are not observed.

Microevolutionary changes do not modify basic types; rather,
they serve to adapt organisms within their types. Change
is subservient to stasis on a higher level.

One could argue at this point that such 'minor' changes, extrapolated
over millions of years, could result in macroevolutionary change.
But the observational evidence will not support this argument.
In the bacterial example just given, the ribosome did not deviate
from the prokaryotic type to which it belonged. In fact, even
the novel metabolic capabilities discovered by Barry Hall's research
with E. coli (Hall, 1983) cannot be said to have transformed
these bacteria into a new species. And certainly, the boundaries
of the bacterial type to which E. coli belong have not
been violated. Thus, the changes observed in the laboratory are
not analogous to the sort of changes needed for macroevolution.
Those who argue from microevolution to macroevolution may be guilty,
then, of employing a false analogy--especially when one considers
that microevolution may be a force of stasis, not transformation
.

The fifth level of stasis is natural selection. For purposes
of clarity, Kimura (1983: 118) classifies natural selection into
two distinct types, positive and negative selection. Positive,
or directional, selection works to spread an advantageous mutation
or trait throughout a population. Kimura notes that:

Despite its biological importance, positive selection is seldom
observed at work in nature.

Negative, or stabilizing, selection is much more common in
nature. It works to eliminate deleterious mutations or traits.
Kimura notes that when compared to positive selection, examples
of negative selection are much more abundant. Studies of mutations
in Drosophila, for example, have "shown beyond a doubt
that the majority of these mutant genes are unconditionally deleterious
both in homozygous and heterozygous states" (Kimura, 1983:
118).

It should come as no surprise that natural selection works
like this most of the time. Complex organic designs are composed
of interdependent structures, most (or all) of which must be present
simultaneously to offer any selective advantage. Natural selection
acts to eliminate the useless incipient stages through which any
major structural or functional innovation must pass. In so doing,
it inhibits major evolutionary change and promotes stasis. Soren
Lovtrup (1987: 274) reminds us that this criticism of Darwinism
is longstanding:

Darwin complained that his critics did not understand him,
but he did not seem to realize that almost everybody, friends,
supporters and critics, agreed on one point, his natural selection
cannot account for the origin of the variations, only for their
possible survival. And the reasons for rejecting Darwin's proposal
were many, but first of all that many innovations cannot possibly
come into existence through accumulation of many small steps,
and even if they can, natural selection cannot accomplish it,
because incipient and intermediate stages are not advantageous.

For those who must describe the history of life as a purely
natural phenomenon, the winnowing action of natural selection
is truly a difficult problem to overcome. For scientists who are
content to describe accurately those processes and phenomena which
occur in nature (in particular, stasis), natural selection acts
to prevent major evolutionary change.

This aspect of selection correlates well with the fossil record.
Fossil evidence indicates that phyla stopped appearing first,
followed by classes and then orders. All modern phyla, for example,
can be traced to the early Cambrian, and no new phylum has arisen
in over 500 million years. One explanation for this pattern holds
that novel body plans are excluded by competition and the lack
of open adaptive space; thus, natural selection prevents major
evolutionary change and promotes stasis.

Conclusion and Prospects for Research

I have suggested possible mechanisms to account for the stasis
observed in fossil and molecular data (see Table I). These mechanisms
work at different levels, from gene sequences at one end to populations
on the other (Figure 3). As a mutation travels through each level
of stasis, less and less real transformation is likely to be realized.
When one considers the already extemely slow process of neo-Darwinian
evolution, macroevolution--which requires novel structures and
functions--seems unlikely.

Given the overwhelming preoccupation with demonstrating change,
it is remarkable that possible mechanisms for stasis are relatively
easy to find. One can only wonder how our theoretical and explanatory
landscape would appear, if even a small fraction of the energy
spent on supporting theories of continuity were instead spent
on examining the various phenomena of discontinuity.

Perhaps the most exciting point about hypotheses of stasis
is that, unlike theories of macroevolution, they are all testable
and subject to experimental falsification.

Site-directed mutagenesis can be used to test notions of functional
constraint in proteins, to determine whether supposed evolutionary
transformations are possible.

The exact relationship between mutations and the protein degradation
systems can be examined. The cytoplasmic regulatory molecules
can be sought experimentally, and their role in gene expression
studied. One could even predict that certain genes may be more
resistant to mutation than other genes. It has already been determined
that actual mutation rates appear to differ among different genes
(Wolfe et al., 1989). The list can go on, but it is clear that
there is much room for genuine scientific research into the possible
mechanisms of stasis.

It is time to take stasis seriously, regardless of its philosophical
implications, and attempt to account for it through rigorous scientific
research.

Michael Thomas, a Ph.D. student in molecular
biology, is currently working on a book outlining the discontinuities
between basic cell types. He has a longstanding interest in origins
issues. Correspondence may be addressed to M. Thomas, c/o Access
Research Network, P.O. Box 38069, Colorado Springs, CO 80937-8069.